When to intubate in GCS?

GCS ≤ 8 requires intubation for airway protection. The patient cannot protect their own airway at this level of consciousness. Motor score is the most prognostically important component.

What is the best initial fluid for sepsis resuscitation?

Lactated Ringer's (LR) is the preferred resuscitation fluid. The SMART trial (2018) showed balanced crystalloids reduced death, new renal failure, and persistent renal dysfunction compared to normal saline.

When to start vasopressors in septic shock?

Start norepinephrine (first-line vasopressor) if MAP remains < 65 mmHg after initial 30 mL/kg crystalloid resuscitation, or earlier if patient is profoundly hypotensive. Do not delay pressors to complete full fluid resuscitation.

Why can serum uric acid be normal during acute gout?

During acute inflammation, IL-6 increases renal urate excretion and redistributes urate from plasma to tissues. Up to 40% of acute gout flares have normal serum uric acid. Joint aspiration with polarized microscopy is needed for definitive diagnosis.

How do you distinguish lupus flare from infection in SLE?

Key clues: CRP is low/normal in flare but elevated in infection. Complement (C3/C4) drops in flare but is normal/elevated in infection. Procalcitonin is elevated in bacterial infection but normal in flare. Anti-dsDNA rises in flare, stable in infection.

What is the difference between DKA and HHS?

DKA features acidosis (pH 600), hyperosmolality (> 320), and minimal ketosis -typically in Type 2 DM. DKA requires insulin drip; HHS requires aggressive fluid resuscitation first.

When to give tPA in acute ischemic stroke?

IV alteplase (tPA) can be given within 4.5 hours of last known well time in eligible patients. CT head must rule out hemorrhage first. For large vessel occlusion, mechanical thrombectomy can be performed up to 24 hours with favorable imaging.

What antibiotics for community-acquired pneumonia?

Inpatient non-ICU: ceftriaxone + azithromycin. ICU: ceftriaxone + azithromycin (add vancomycin if MRSA risk). Outpatient healthy: amoxicillin. Outpatient with comorbidities: augmentin + azithromycin or respiratory fluoroquinolone. Duration: 5 days if clinically stable for 48 hours.

How to interpret iron studies?

Iron deficiency: low ferritin (< 30), high TIBC, low iron, low transferrin saturation (< 20%). Anemia of chronic disease: normal/high ferritin (acute phase reactant), low TIBC, low iron. A ferritin of 50-100 in an inflamed patient may still represent iron deficiency.

What is the correction rate for hyponatremia?

Correct sodium no more than 8 mEq/L in 24 hours to avoid osmotic demyelination syndrome (ODS). For symptomatic severe hyponatremia with seizures, give 3% hypertonic saline 100-150 mL bolus over 10-20 minutes. If overcorrected, use D5W + DDAVP rescue protocol.

When to start antibiotics in meningitis?

Within 30-60 minutes. Do NOT delay antibiotics for LP or CT. Draw blood cultures, start empiric antibiotics (vancomycin + ceftriaxone ± ampicillin if > 50 or immunocompromised), then perform LP when possible. Dexamethasone should be given before or with the first antibiotic dose.

DOACs vs warfarin in antiphospholipid syndrome?

DOACs are contraindicated in APS. The TRAPS trial (2018) showed rivaroxaban was inferior to warfarin with more thrombotic events in triple-positive APS patients. Warfarin with INR target 2-3 is the standard for APS, indefinitely.

How to manage scleroderma renal crisis?

ACE inhibitors (captopril) are life-saving -start immediately and titrate aggressively. Do NOT hold for rising creatinine. Steroids > 15 mg prednisone per day precipitate scleroderma renal crisis. ARBs are NOT a substitute -evidence is only for ACEi.

What are the 4 pillars of heart failure treatment?

Guideline-directed medical therapy (GDMT) for HFrEF: (1) ARNI or ACEi/ARB, (2) beta-blocker (carvedilol, metoprolol succinate, or bisoprolol), (3) MRA (spironolactone or eplerenone), (4) SGLT2 inhibitor (dapagliflozin or empagliflozin). All four should be initiated and titrated to target doses.

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EMERGENTEndocrine

Pheochromocytoma

Catecholamine-secreting tumor of the adrenal medulla. Rule of 10s: 10% bilateral, 10% extra-adrenal (paraganglioma), 10% malignant, 10% familial. Alpha-block BEFORE beta-block.

🔍 Overview

Overview

Pheochromocytoma is a catecholamine-secreting neuroendocrine tumor arising from chromaffin cells of the adrenal medulla. Extra-adrenal tumors = paragangliomas (arise from sympathetic ganglia -organ of Zuckerkandl most common). Classic presentation: paroxysmal triad of headache + sweating + palpitations with hypertension. Accounts for < 1% of hypertension but must be considered in: resistant HTN, hypertensive crisis with paroxysms, adrenal incidentaloma, familial syndromes (MEN2A/2B, VHL, NF1, SDH mutations). "Rule of 10s": 10% bilateral, 10% extra-adrenal, 10% malignant, 10% pediatric, ~40% familial (higher than classically taught). The critical teaching point: Alpha-blockade MUST precede beta-blockade -unopposed alpha stimulation during beta-blockade → hypertensive crisis.

🧪 Workup

Workup

Plasma free metanephrines -best initial screening test. Sensitivity > 97%. Elevated metanephrine (from epinephrine) or normetanephrine (from norepinephrine). Draw with patient supine × 30 min. Lenders et al., Endocrine Society 2014
24-hour urine metanephrines + catecholamines -confirmatory if plasma equivocal. Also useful for monitoring post-resection.
CT abdomen/pelvis with contrast -localize adrenal mass. Pheos are typically > 3 cm, heterogeneous, > 10 HU on non-contrast CT (lipid-poor), enhance avidly.
MRI abdomen -alternative. Classic "light bulb" bright signal on T2-weighted images. Preferred in pregnancy, children, and known SDH mutations.
MIBG scan (I-123) -functional imaging for metastatic disease, extra-adrenal paragangliomas, or recurrence. If MIBG negative → FDG-PET or Ga-68 DOTATATE PET.

Monitoring

🚨 Management

Management

Step 1 -Alpha-blockade (start 10-14 days before surgery):
- Phenoxybenzamine 10 mg BID → titrate to 20-30 mg BID (non-competitive, irreversible alpha-blocker -gold standard pre-op). Target: seated BP < 130/80 with standing SBP > 90. [Lenders et al., Endocrine Society 2014
- Alternative: doxazosin 2-8 mg daily (competitive alpha-1 blocker -shorter acting, less reflex tachycardia).
Step 2 -Beta-blockade (ONLY after adequate alpha-blockade): Start 2-3 days before surgery or once HR > 100 on alpha-blocker. Propranolol 20-40 mg TID or atenolol 25-50 mg daily. Controls reflex tachycardia from alpha-blockade.
Step 3 -Volume expansion: High-sodium diet + liberal fluids in the 1-2 weeks pre-op. Chronic catecholamine excess → vasoconstriction → intravascular volume depletion. Volume resuscitation prevents post-resection hypotension.
Step 4 -Surgery: Laparoscopic adrenalectomy is definitive treatment. Intraoperative: expect BP swings during tumor manipulation → have nitroprusside (for hypertensive surges) and phenylephrine (for hypotension post-ligation) ready.
Hypertensive crisis management: Phentolamine 2-5 mg IV q5min (competitive alpha-blocker) or nicardipine drip. NEVER give beta-blocker alone -unopposed alpha → worse hypertension.

⚠ ALPHA BEFORE BETA -always. Beta-blockade alone removes beta-2 vasodilation → unopposed alpha-1 vasoconstriction → lethal hypertensive crisis. This is one of the most tested principles in endocrinology. Goldstein et al., 1999

💊 Medications

Medications

Drug	Dose	Route	Notes
Phenoxybenzamine	10 mg BID → titrate to 20-30 mg BID	PO	Non-competitive alpha-blocker. Start 10-14 days pre-op. Irreversible -long duration. Orthostatic hypotension, nasal congestion, reflex tachycardia.
Doxazosin	2-8 mg daily	PO	Competitive alpha-1 blocker. Shorter acting than phenoxybenzamine. Less tachycardia. Some centers prefer.
Propranolol	20-40 mg TID	PO	ONLY after alpha-blockade established. Controls reflex tachycardia. Start 2-3 days before surgery.
Metyrosine	250 mg QID (max 4g/day)	PO	Tyrosine hydroxylase inhibitor -blocks catecholamine synthesis. For refractory hypertension or inoperable tumors. Sedation, EPS side effects.
Phentolamine	2-5 mg IV q5min PRN	IV	Hypertensive crisis. Competitive alpha-blocker. Fast onset. Have ready in OR during tumor manipulation.
Nicardipine	5-15 mg/hr IV	IV drip	Alternative for intraoperative/crisis BP control. Smooth, titratable.

🏥 Rounds

Pimp Questions

❓ Why must you alpha-block BEFORE beta-blocking in pheochromocytoma?

Beta-2 receptors cause vasodilation. If you block them with a beta-blocker while catecholamines are still high, you remove the vasodilatory counterbalance → unopposed alpha-1 vasoconstriction → severe hypertensive crisis. Alpha-blockade first reduces the vasoconstriction, then beta-blockade safely controls the reflex tachycardia. This is one of the most tested principles in endocrinology.

❓ What is the best initial screening test for pheochromocytoma?

Plasma free metanephrines. Sensitivity > 97% -best rule-out test. Metanephrine (from epinephrine) and normetanephrine (from norepinephrine) are continuously produced by tumor metabolism (not just during paroxysms), making them more reliable than catecholamine levels. Draw with patient supine × 30 min to avoid false positives from sympathetic activation. Lenders, 2014

❓ Why should you NOT biopsy a suspected pheochromocytoma?

Needle insertion into the tumor causes massive catecholamine release → hypertensive crisis, arrhythmia, MI, stroke, death. Diagnosis is made by biochemistry (metanephrines) + imaging. If you see an adrenal mass and pheo is in the differential, rule out pheo biochemically BEFORE any invasive procedure.

❓ What percentage of pheochromocytomas are hereditary and what syndromes should you screen for?

Up to 40% have a germline mutation (much higher than the historical "10%"). Key syndromes: MEN2A/2B (RET mutation -pheo + medullary thyroid carcinoma ± hyperparathyroidism), VHL (hemangioblastomas + renal cell + pheo), NF1 (neurofibromas + pheo), SDHx mutations (paraganglioma-pheochromocytoma syndrome -most common hereditary cause). Genetic testing recommended for ALL patients.

❓ What happens to blood glucose immediately after pheochromocytoma resection?

Hypoglycemia. Catecholamines suppress insulin secretion and stimulate gluconeogenesis/glycogenolysis. After tumor removal, the catecholamine-mediated insulin suppression is abruptly removed → rebound hyperinsulinemia → hypoglycemia. Monitor glucose q1-2h for 24h post-op. Have D50 ready.

❓ What blood pressure pattern on ambulatory monitoring suggests pheochromocytoma?

Paroxysmal hypertension with intervening normotension or hypotension. Also: loss of nocturnal dipping (BP stays elevated at night instead of the normal 10-20% drop). Some patients present with orthostatic hypotension -paradoxically, chronic catecholamine excess → receptor downregulation + volume depletion → orthostasis between paroxysms.

Clinical Examples

📋 Case 1, Classic Pheochromocytoma with Paroxysmal HTN

Patient: 38F with episodic headaches, diaphoresis, and palpitations × 4 months. Episodes last 20-30 min, occur 3-4×/week. BP 230/120 during episode, 140/88 at baseline. HR 128 during episode. Resistant to 3 antihypertensives.

Key findings: Classic paroxysmal triad (headache + diaphoresis + palpitations). Plasma free metanephrines: metanephrine 420 pg/mL (elevated), normetanephrine 2100 pg/mL (markedly elevated). CT: 3.5 cm right adrenal mass, 35 HU.

Management:

Phenoxybenzamine 10 mg PO BID → titrate to goal BP < 130/80 seated with orthostatic SBP > 90 standing
High-salt diet + liberal fluids (catecholamine-induced volume contraction, must volume-expand before surgery)
Add beta-blocker (propranolol 20 mg TID) ONLY after adequate alpha-blockade (3-5 days minimum)
NEVER give beta-blocker first → unopposed alpha stimulation → hypertensive crisis
Laparoscopic adrenalectomy after 10-14 days of medical optimization

Teaching point: Alpha before beta, the cardinal rule of pheo management. Beta-blockers without alpha-blockade remove beta-2 vasodilation, leaving unopposed alpha vasoconstriction, causing severe hypertensive crisis.

📋 Case 2, Pheo Crisis in the OR

Patient: 52M undergoing cholecystectomy. During insufflation, sudden BP 280/160, HR 160, SVT on telemetry. No known pheo history. Incidental 2.8 cm adrenal mass seen on pre-op CT but not investigated.

Key findings: Intraoperative catecholamine crisis, triggered by abdominal insufflation compressing an undiagnosed pheochromocytoma. Surgical manipulation is the classic precipitant of pheo crisis.

Management:

Phentolamine 2-5 mg IV bolus q5min until BP controlled (fast-acting alpha-blocker for crisis)
Nicardipine drip 5-15 mg/hr as alternative/adjunct for BP control
Esmolol drip for rate control ONLY after alpha-blockade initiated
Abort the primary surgery, do not manipulate the adrenal gland
Post-op: confirm diagnosis with plasma metanephrines, plan formal pheo workup and staged adrenalectomy after medical optimization

Teaching point: Adrenal incidentalomas > 1 cm should always have plasma metanephrines checked before any surgery. An undiagnosed pheo in the OR has a mortality rate of up to 80% if unrecognized.

📋 Case 3, Hereditary Paraganglioma (SDH Mutation)

Patient: 24M with HTN and headaches. Father had bilateral pheos at age 30. Plasma normetanephrine 980 pg/mL. MRI: 2.2 cm left extra-adrenal retroperitoneal mass (paraganglioma). Right adrenal normal.

Key findings: Young age + family history + extra-adrenal location = high suspicion for hereditary syndrome. ~40% of pheos/paragangliomas have germline mutations (SDHx, VHL, MEN2, NF1).

Management:

Genetic testing: SDHx panel, VHL, RET (MEN2), NF1, mandatory for all pheos/paragangliomas per Endocrine Society
MIBG scintigraphy or Ga-68 DOTATATE PET/CT to rule out multifocal/metastatic disease
Alpha-blockade → surgical resection of paraganglioma
Lifelong annual screening with plasma metanephrines (high recurrence/new primary risk with SDH mutations)
Screen first-degree relatives if mutation confirmed

Teaching point: All pheos/paragangliomas should get genetic testing, 40% are hereditary. SDHx mutations carry the highest malignancy risk (up to 40% for SDHB). Extra-adrenal location and young age are red flags for hereditary syndromes.

Sample Presentation

Mr. Park is a 42-year-old man presenting with episodic headaches, diaphoresis, and palpitations × 6 months. Episodes last 15-30 min, occur 2-3 times per week, associated with severe hypertension (240/130 during episodes, 155/95 baseline). Home medications: amlodipine 10 mg, lisinopril 40 mg, HCTZ 25 mg (resistant HTN). Labs: plasma normetanephrine 1850 pg/mL (> 4× ULN). CT abdomen: 4.2 cm right adrenal mass, heterogeneous enhancement, 38 HU on non-contrast.

Key Points: Classic pheo -paroxysmal triad + resistant HTN + markedly elevated normetanephrine + lipid-poor adrenal mass. Start phenoxybenzamine 10 mg BID immediately. Titrate over 10-14 days. High-sodium diet for volume expansion. Add propranolol ONLY after adequate alpha-blockade. Genetic testing. Laparoscopic adrenalectomy after medical optimization.

BP (standing + seated) daily during alpha-blockade titration -target: seated < 130/80, standing SBP > 90 mmHg (orthostatic tolerance confirms adequate blockade)
HR -if > 100 on alpha-blocker → start beta-blocker (after adequate alpha-blockade confirmed)
Pre-op checklist: BP controlled × 7-14 days, mild orthostatic hypotension present, HR 60-80, no ECG ischemia, no new ST changes × 2 weeks
Intraoperative: arterial line mandatory. Expect BP surges during tumor manipulation → phentolamine/nitroprusside ready. Expect hypotension after tumor ligation → volume + phenylephrine/vasopressin ready.
Post-op glucose -hypoglycemia is common after tumor removal (catecholamines were suppressing insulin → insulin rebound). Monitor glucose q1-2h × 24h.
Post-op plasma metanephrines -at 2-4 weeks. Should normalize. If persistently elevated → residual/metastatic disease.
Annual biochemical screening -lifelong (recurrence risk ~5-10%). More frequent if genetic syndrome.
Genetic counseling -all patients. Screen first-degree relatives if mutation found.

Monitoring

📋 Summary

Summary

Triad

Headache + sweating + palpitations with paroxysmal hypertension

Screen

Plasma free metanephrines (sensitivity > 97%). 24h urine for confirmation.

Imaging

CT/MRI adrenal → MIBG or DOTATATE PET for extra-adrenal/metastatic

Treatment

Alpha-block × 10-14d → beta-block → volume expand → surgery.

Never Do

Beta-block alone. Biopsy the mass. Skip genetic testing.

Post-Op

Monitor glucose (hypoglycemia). Metanephrines at 2-4 wk. Annual screening lifelong.

📄 One Pager

One-Pager

Pheochromocytoma

Alpha before Beta. Always.

Pre-Op Protocol

Day 1-14: Phenoxybenzamine 10 mg BID → titrate. Day 10+: Add propranolol ONLY after alpha adequate. Diet: high sodium + fluids. Goal: BP < 130/80 seated, SBP > 90 standing. OR ready: phentolamine + nitroprusside + phenylephrine.

Red Flags

Do NOT biopsy (catecholamine crisis). Do NOT beta-block first (unopposed alpha → crisis). 40% hereditary → always genetic test. Post-op hypoglycemia -monitor glucose q1-2h × 24h.

Trials

Lenders 2014 (plasma metanephrines screening) · Endocrine Society Pheo Guidelines 2014